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首页> 外文期刊>American Journal of Physiology >Participation of prostaglandin E receptor EP4 subtype in duodenal bicarbonate secretion in rats.
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Participation of prostaglandin E receptor EP4 subtype in duodenal bicarbonate secretion in rats.

机译：前列腺素E受体EP4亚型参与大鼠十二指肠碳酸氢盐的分泌。

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摘要

We examined, by using a specific PGE receptor subtype EP4 agonist and antagonist, the involvement of EP4 receptors in duodenal HCO(3)(-) secretion induced by PGE(2) and mucosal acidification in rats. Mucosal acidification was achieved by exposing a duodenal loop to 10 mM HCl for 10 min, and various EP agonists were given intravenously 10 min before the acidification. Secretion of HCO(3)(-) was dose-dependently stimulated by AE1-329 (EP4 agonist), the maximal response being equivalent to that induced by sulprostone (EP1/EP3 agonist) or PGE(2). The stimulatory action of AE1-329 and PGE(2) but not sulprostone was attenuated by AE3-208, a specific EP4 antagonist. This antagonist also significantly mitigated the acid-induced HCO(3)(-) secretion. Coadministration of sulprostone and AE1-329 caused a greater secretory response than either agent alone. IBMX potentiated the stimulatory action of both sulprostone and AE1-329, whereas verapamil mitigated the effect of sulprostone but not AE1-329. Chemical ablationof capsaicin-sensitive afferent neurons did not affect the response to any of the EP agonists used. We conclude that EP4 receptors are involved in the duodenal HCO(3)(-) response induced by PGE(2) or acidification in addition to EP3 receptors. The process by which HCO(3)(-) is secreted through these receptors differs regarding second-messenger coupling. Stimulation through EP4 receptors is mediated by cAMP, whereas that through EP3 receptors is regulated by both cAMP and Ca(2+); yet there is cooperation between the actions mediated by these two receptors. The neuronal reflex pathway is not involved in stimulatory actions of these prostanoids.
机译：我们通过使用特定的PGE受体亚型EP4激动剂和拮抗剂，检查了EP4受体参与由PGE（2）和大鼠黏膜酸化引起的十二指肠HCO（3）（-）分泌。黏膜酸化是通过将十二指肠环暴露于10 mM HCl中10分钟来实现的，在酸化之前10分钟静脉内给予各种EP激动剂。 HCO（3）（-）的分泌受到AE1-329（EP4激动剂）的剂量依赖性刺激，最大反应与舒普司通（EP1 / EP3激动剂）或PGE（2）诱导的反应相同。 AE1-329和PGE（2）的刺激作用，但不是舒普司通，被AE3-208（一种特定的EP4拮抗剂）减弱。该拮抗剂还显着减轻了酸诱导的HCO（3）（-）分泌。沙普前列酮和AE1-329的共同给药比单独的任何一种药物引起更大的分泌反应。 IBMX增强了舒普洛司通和AE1-329的刺激作用，而维拉帕米减轻了舒普洛司通的作用而不是AE1-329。辣椒素敏感性传入神经元的化学消融不影响对使用的任何EP激动剂的反应。我们得出的结论是，除EP3受体外，EP4受体还参与了由PGE（2）或酸化诱导的十二指肠HCO（3）（-）反应。通过这些受体分泌HCO（3）（-）的过程在第二信使偶联方面有所不同。通过EP4受体的刺激是由cAMP介导的，而通过EP3受体的刺激则受cAMP和Ca（2+）的调节。然而，由这两种受体介导的作用之间存在协同作用。神经元反射途径不参与这些前列腺素类的刺激作用。

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